Neostigmin und Edrophonium : Antagonisierung einer tiefen und oberflächlichen Mivacuriumblockade

Mivacurium has a short duration of action because it is rapidly hydrolysed by plasma cholinesterase.There is ongoing controversy concerning the antagonism of mivacurium-induced neuromuscular block,firstly because of its short spontaneous recovery time, and secondly because the metabolism of mivacurium may be inhibited by anticholinesterases.We therefore compared neostigmine and edrophonium reversal of deep and moderate mivacurium-induced blocks. Methods: After approval by the local ethics committee, 48 ASA class I and II adult patients were investigated during nitrous oxide-fentanyl-thiopental anaesthesia using train-of-four (TOF) stimulation and monitoring of the isometric force of adduction ofa a thumb. The patients received 0.2 mg/kg mivacurium i.v. Neuromuscular transmission was allowed to recover spontaneously in 10 patients (group SP). In 2 other groups the neuromuscular block was antagonised by administration of 0.04 mg/kg neostigmine (group N5; n=9) or 1.0 mg/kg edrophonium (group E5;n=10) when T1 had recovered spontaneously to 5% of control. In two other groups the neuromuscular block was antagonised with the same doses of neostigmine or edrophonium in 10 patients (group N25) and 9 patients (group E25), respectively, when T1 had recovered spontaneously to 25% of control. Results: Neostigmine or edrophonium administered when T1 had recovered spontaneously to 25% of control shortened the recovery time (time from administration of antagonist to a T4/T1-ratio of 0.7) significantly from 10.7±2.2 min (mean±SD) in the SP group to 5.1±2.0 and 5.3±1.5 min in the N25 and E25 groups, respectively (P<0.05). The corresponding recovery times in the SP, N5,and E5 groups were 15.9±2.9, 10.0±1.9, and 7.7±2.2 min, respectively. The difference between the SP and E5 groups was significant (P<0.05).The recovery indices (time from 25% to 75% recovery of T1) of 3.0±1.3 and 1.7±0.9 min for the E5 and E25 groups, respectively, were shorter than those of the SP group at 6.1±2.0 min (P<0.05). Conclusions: Two theoretical reasons, the very rapid onset time and the fact that it does not inhibit plasma cholinesterase,suggest edrophonium to be the preferred antagonist of a mivacurium-induced blockade. These two characteristics are reflected in our results:only edrophonium was able to shorten the recovery index significantly and, administered at a profound level of mivacurium-induced neuromuscular block, only edrophonium was successful in shortening recovery time significantly. Therefore, edrophonium should be the anticholinesterase of choice to antagonise a mivacurium-induced neuromuscular block.